The development of mammalian
nonalcoholic fatty liver disease is associated with oxidative stress, reduced mitochondrial function, and increased apoptosis in hepatocytes; however, the expressions of mitochondria-related genes are elevated in goose
fatty liver, suggesting that there may be a unique protective mechanism in goose
fatty liver. The aim of the study was to investigate this protective mechanism in terms of
anti-oxidant capacity. Our data showed no substantial differences in the
mRNA expression levels of the apoptosis-related genes including B-cell lymphoma-2 (Bcl-2), BCL2-associated X (Bax), cysteinyl
aspartate-specific proteinase-3 (Caspase-3), and cysteinyl
aspartate-specific proteinase-9 (Caspase-9) in the livers of the control and overfeeding Lander geese groups. The
protein expression levels of
Caspase-3 and cleaved
Caspase-9 were not markedly different between the groups. Compared with the control group,
malondialdehyde content was significantly lower (P < 0.01),
glutathione peroxidase (GSH-Px) activity,
glutathione (GSH) content, and mitochondrial membrane potential levels were higher (P < 0.01) in the overfeeding group. The
mRNA expression levels of the
anti-oxidant genes
superoxide dismutase 1 (SOD1),
glutathione peroxidase 1 (GPX1), and
glutathione peroxidase 2 (GPX2) were increased in goose primary hepatocytes after 40 mM and 60 mM
glucose treatment.
Reactive oxygen species (ROS) levels were significantly reduced (P < 0.01), whereas the mitochondrial membrane potential was maintained at normal levels. The
mRNA expression levels of the apoptosis-related genes Bcl-2, Bax, and
Caspase-3 were not substantial. There were no significant differences in the expression levels of
Caspase-3 and cleaved
Caspase-9 proteins. In conclusion,
glucose-induced enhanced
anti-oxidant capacity may help protect the function of mitochondria and inhibit the occurrence of apoptosis in goose
fatty liver.